title: Increased left ventricular mass and decreased left ventricular systolic function have independent pathways to ventricular arrhythmogenesis in coronary artery disease.
abstract: BACKGROUND
  Following myocardial infarction, individual patients can have wide variations in the extent of left ventricular systolic dysfunction (LVSD) and increased left ventricular (LV) mass. Both affect the risk for sudden cardiac death, but only LV ejection fraction is used for risk prediction.
  
  
  OBJECTIVE
  The purpose of this study was to evaluate the independent as well as the additive contributions of increased LV mass and decreased LV ejection fraction to sudden cardiac death in the general population.
  
  
  METHODS
  In the ongoing Oregon Sudden Unexpected Death Study, we studied consecutive SCD cases (n = 191) and coronary artery disease controls (n = 203) from the Portland, Oregon, metropolitan area (population approximately 1,000,000; 2002-2008). Comparisons of echocardiographic LV mass obtained prior and unrelated to sudden cardiac death (SCD) were conducted, and a logistic regression model was used to evaluate the relationship between SCD, severe LVSD, LV mass, and other relevant clinical variables.
  
  
  RESULTS
  In a multivariate model, both severe LVSD and left ventricular hypertrophy (LVH) were associated with increased SCD risk (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 for severe LVSD; OR 1.8, 95% CI 1.1-2.9 for LVH). In patients with coexisting severe LVSD and LVH, risk of SCD was additive (OR 3.5, 95% CI 1.7-7.2). In the same model, increased age, atrial fibrillation/flutter, elevated creatinine, and diabetes independently increased risk, and use of angiotensin receptor blockers attenuated risk.
  
  
  CONCLUSIONS
  Reduced LV ejection fraction and increased LV mass had independent and additive effects on risk of sudden death. Despite the significant overlap between the two conditions, these findings point toward the existence of independent mechanistic pathways for ventricular arrhythmias that occur due to LVSD and LVH.
authors.affiliation: Heart Institute, Cedars-Sinai Medical Center, Los Angeles California, USA.
authors.forename: Kyndaron
authors.initials: K
authors.lastname: Reinier
authors.forename: Celia
authors.initials: C
authors.lastname: Dervan
authors.forename: Tejwant
authors.initials: T
authors.lastname: Singh
authors.forename: Audrey
authors.initials: A
authors.lastname: Uy-Evanado
authors.forename: Shenghan
authors.initials: S
authors.lastname: Lai
authors.forename: Karen
authors.initials: K
authors.lastname: Gunson
authors.forename: Jonathan
authors.initials: J
authors.lastname: Jui
authors.forename: Sumeet S
authors.initials: SS
authors.lastname: Chugh
mesh_terms: D000368:Aged; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000473:pathology / Q000503:physiopathology*; D016757:Death, Sudden, Cardiac / Q000453:epidemiology / Q000473:pathology; D005260:Female; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000473:pathology / Q000503:physiopathology*; D016015:Logistic Models; D008297:Male; D018570:Risk Assessment; D012307:Risk Factors; D013318:Stroke Volume / Q000502:physiology*; D013599:Systole / Q000502:physiology; D014463:Ultrasonography; D018487:Ventricular Dysfunction, Left / Q000453:epidemiology / Q000473:pathology / Q000503:physiopathology*